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Flashcards in packet 3 Deck (30)
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1
Q

Action potentials of all active cells can be detected and recorded

A

EKG

2
Q

atrial depolarization

* muscle contraction signal

A

P wave

3
Q

conduction time from atrial to ventricular excitation

A

P to Q interval

4
Q

ventricular depolarization

*stronger action potential

A

QRS complex

5
Q

ventricular repolarization

A

T wave

6
Q

At 75 beats/min, one cycle requires 0.8 sec.
End diastolic volume (EDV)
End systolic volume (ESV)
Stroke Volume (SV)

A

one cardiac cycle

7
Q

volume in ventricle at end of diastole, about 130ml

A

end diastolic volume

8
Q

volume in ventricle at end of systole, about 60ml

A

end systolic volume

9
Q

the volume ejected per beat from each ventricle, about 70ml

SV = EDV - ESV

A

stroke volume

10
Q

brief period when volume in ventricles does not change– ventricles relax, pressure drops and AV valves open

A

Isovolumetric relaxation

11
Q

as blood flows from full atria
diastasis: as blood flows from atria in smaller volume
atrial systole pushes final 20-25 ml blood into ventricle

A

Ventricular filling

12
Q

ventricular systole
isovolumetric contraction
ventricular ejection: as SL valves open and blood is ejected

A

ventricular systole

13
Q

erratic heartbeat, uncoordinated contractions

A

fibrillation

14
Q

interference with AV node  erratic, incomplete atrial contractions. Often secondary to other heart problem, and rarely life-threatening.
Treatment: drug/electro-cardioconversion; anti-coagulants
Symptoms: none, palpitations, fainting, nausea, chest pain; can lead to stroke and congestive heart failure.

A

atrial fibrillation

15
Q

erratic, incomplete ventricular contractions. Immediately life-threatening due to lack of somatic, pulmonary, and cardiac circulation; often secondary to other heart disease.
Symptoms: sudden collapse; death often first “symptom.”
Treatment: electric cardioconversion, then treat underlying issue

A

ventricular fibrillation

16
Q

rapid (especially ventricular) heartbeat.
Symptoms: range from faintness, short-of-breath to sudden death, depending location and cause.
Treatment: drug or electric cardioconversion, then treat underlying issue

A

Tachycardia

17
Q

slows heartbeat

A

bradycardia

18
Q

Blood pressure in aorta is 120mm Hg
Blood pressure in pulmonary trunk is 30mm Hg
Differences in ventricle wall thickness allows heart to push the same amount of blood with more force from the left ventricle
The volume of blood ejected from each ventricle is 70ml (stroke volume)

A

ventricular pressures

19
Q

mL blood pumped/min

= mL blood/beat x beat/min

A

cardiac output

20
Q

70mL/beat x 75 beat/min = 5.25L

(thus blood moves through body 1x/min!)

A

normal CO

21
Q

regulate stroke volume by allowing more blood in the ventricle and/or stronger contractions). Upper limit = size of ventricle and time allowed to fill.

A

more blood/beat

22
Q

increase heart rate). Upper limit = need to reinitiate beat (refractory period)

A

more beats/min

23
Q

Nervous system control

A

Sensors
sympathetic NS
Parasympatheitc NS

24
Q

limbic system, baroreceptors, chemoreceptors, proprioreceptors. Feed into medulla’s cardiovascular center (medulla). Control through ANS.

A

sensors

25
Q

nerves connect with SA & AV nodes and myocardium. HORMONE? increases rate of autorhythmic SA firing and uptake of Ca++ ( contractility) by all muscle cells.

A

sympathetic NS

26
Q

nerves (CN???) connect with SA & AV nodes and myocardium of atria. Decreases rate of autorhythmic firing with ACh.

A

parasympathetic NS

27
Q

What controls heart rate and blood pressure

A

Nervous system
endocrine system
cation control
metabolic control

28
Q

Adrenal medulla (responding to hypothalamus) releases epinephrine and norepinephrine = increase of autorhythmic rate and contractility.

A

endocrine system

29
Q

Increased K+ prevents action potential
Increased Na+ blocks Ca++ entry
Increased Ca++ boost contractility, rate

A

cation control

30
Q

Increased H+ (acidosis) or OH– decrease heart rate.

A

metabolic control